Abstract
Diabetes is a major risk factor for the development of cardiovascular disease with a higher incidence of myocardial infarction. This study explores the role of metformin, a first-line antihyperglycemic agent, in postinfarction fibrotic and inflammatory remodeling in mice. Three-month-old C57BI/6J mice were submitted to 30 min cardiac ischemia followed by reperfusion for 14 days. Intraperitoneal treatment with metformin (5 mg/kg) was initiated 15 min after the onset of reperfusion and maintained for 14 days. Real-time PCR was used to determine the levels of COL3A1, αSMA, CD68, TNF-α and IL-6. Increased collagen deposition and infiltration of macrophages in heart tissues are associated with upregulation of the inflammation-associated genes in mice after 14 days of reperfusion. Metformin treatment markedly reduced postinfarction fibrotic remodeling and CD68-positive cell population in mice. Moreover, metformin resulted in reduced expression of COL3A1, αSMA and CD68 after 14 days of reperfusion. Taken together, these results open new perspectives for the use of metformin as a drug that counteracts adverse myocardial fibroticand inflammatory remodeling after MI.
Highlights
Diabetes mellitus is a major risk factor for the incidence of myocardial infarction (MI)and cardiovascular morbidity and mortality [1]
Post-MI cryosections of the hearts were stained by both wheatgerm agglutinin (WGA) and Sirius Red
UncerMetformin, the mosttowidely prescribed drug therapyblood for type 2 diabetes mellitus (T2D), has levels pleiotropic benetainty still exists with regard to its effects on reactive cardiac remodeling linked to heart failure (HF)
Summary
Diabetes mellitus is a major risk factor for the incidence of myocardial infarction (MI)and cardiovascular morbidity and mortality [1]. Diabetes mellitus is a major risk factor for the incidence of myocardial infarction (MI). Patients with diabetes have over twice the risk of developing heart failure (HF) than patients without diabetes mellitus [2]. Experimental and clinical investigations suggest that the diabetic heart is more sensitive to ischemic injury than the nondiabetic heart [3]. Myocardial ischemia/reperfusion (I/R) injury is a complex pathophysiological event, resulting in serious acute and chronic myocardial damage linked to adverse myocardial remodeling processes [4,5,6]. Patients with diabetes frequently have echocardiographic evidence of adverse myocardial remodeling; both increased left ventricular mass and dilatation have been reported [8], and these phenotypes are well-known predictors of HF
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